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David Baltimore

Researcher at California Institute of Technology

Publications -  882
Citations -  168784

David Baltimore is an academic researcher from California Institute of Technology. The author has contributed to research in topics: RNA & Virus. The author has an hindex of 203, co-authored 876 publications receiving 162955 citations. Previous affiliations of David Baltimore include Thomas Jefferson University & Johns Hopkins University.

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Structure of a cloned circular Moloney murine leukemia virus DNA molecule containing an inverted segment: implications for retrovirus integration.

TL;DR: Closed circular Moloney murine leukemia virus (M-MuLV) DNA was prepared from recently infected cells and cloned in a lambda vector, providing explicit information concerning the mechanism by which retrovirus DNA integrates into host cell DNA.
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Oct-2, although not required for early B-cell development, is critical for later B-cell maturation and for postnatal survival.

TL;DR: Oct-2 is not required for the generation of immunoglobulin-bearing B cells but is crucial for their maturation to immunoglOBulin-secreting cells and for another undetermined organismal function.
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Sequential induction of NF-kappa B/Rel family proteins during B-cell terminal differentiation

TL;DR: The protein contents of both the inducible and constitutive NF-kappa B/Rel activities in a pre-B- cell line, 70Z/3, and a mature B-cell line, WEHI 231, suggest that the balance between synthesis and degradation of I kappa B-alpha determines whether a particular cell lineage has constitutive activity.
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Alternative mechanisms for activation of human immunodeficiency virus enhancer in T cells.

TL;DR: It is raised the possibility that infection by herpes simplex virus or adenovirus may directly contribute to the activation of HIV in acquired immunodeficiency syndrome by mechanisms independent of antigenic stimulation in T cells.
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N-terminal mutations activate the leukemogenic potential of the myristoylated form of c-abl.

TL;DR: The smallest of these deletions, delta XB, efficiently transforms lymphoid cells in vitro and causes leukemia in vivo demonstrating that gag sequences are not necessary for abl‐induced leukemogenesis.